1,721,053 research outputs found

    Going Beyond Counting First Authors in Author Co-citation Analysis

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    The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed

    Variations on the Author

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    “Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship

    Appropriate Similarity Measures for Author Cocitation Analysis

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    We provide a number of new insights into the methodological discussion about author cocitation analysis. We first argue that the use of the Pearson correlation for measuring the similarity between authors’ cocitation profiles is not very satisfactory. We then discuss what kind of similarity measures may be used as an alternative to the Pearson correlation. We consider three similarity measures in particular. One is the well-known cosine. The other two similarity measures have not been used before in the bibliometric literature. Finally, we show by means of an example that our findings have a high practical relevance.information science;Pearson correlation;cosine;similarity measure;author cocitation analysis

    Dispelling the Myths Behind First-author Citation Counts

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    We conducted a full-scale evaluative citation analysis study of scholars in the XML research field to explore just how different from each other author rankings resulting from different citation counting methods actually are, and to demonstrate the capability of emerging data and tools on the Web in supporting more realistic citation counting methods. Our results contest some common arguments for the continued use of first-author citation counts in the evaluation of scholars, such as high correlations between author rankings by first-author citation counts and other citation counting methods, and high costs of using more realistic citation counting methods that are not well-supported by the ISI databases. It is argued that increasingly available digital full text research papers make it possible for citation analysis studies to go beyond what the ISI databases have directly supported and to employ more sophisticated methods

    Author Index

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    Biallelic deletion and loss of expression of genes at FRA2G region in tumor derived cell lines.

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    Common fragile sites (CFSs) are regions of chromosome instability, that extend for hundreds or thousands of kilobases, at which gaps or breaks are observed when cells are exposed to appropriate culture conditions and particularly to replication stress (Sutherland et al., 1998). CFSs are expressed, with different frequency, on chromosomes of all analysed individuals and therefore have to be considered a constitutive feature of normal chromosomes. Many evidences suggest that CFSs are causally related to cancer. In fact these sites are localised in chromosome bands recurrently involved in rearrangements in cancer cells (Richards, 2001), are sites of preferential viral integration (e.g. Wilke et al., 1996), and may also be involved in amplification events as the breakage points in breakage-fusion-bridge cycles (Coquelle et al., 1997; Ciullo et al., 2002; Hellman et al., 2002). Recently, authors showed that miRNA genes are frequently located at fragile sites as well as in cancer-associated genomic regions (Colin et al., 2004). Moreover more conclusive evidences supporting the relation between CFSs and tumourigenesis derive from cloning and characterization of some CFSs. Ten CFSs have been molecularly characterised, FRA2G (Limongi et al., 2003), FRA3B (Wilke et al., 1996),FRA6E (Denison et al., 2003), FRA6F (Morelli et al., 2002), FRA7G (Huang et al., 1998), FRA7H (Mishmar et al., 1998), FRA7I (Ciullo et al., 2002), FRA9E (Callahan et al., 2003), FRA16D (Mangelsdorf et al., 2000; Paige et al., 2000; Ried et al., 2000), FRAXB (Artl et al., 2002). Many of them have been associated with cancer-specific rearrangements, frequently deletions, so as with gene inactivation involving known or putative tumor-suppressor (TS) genes mapping in the fragile regions. FRA2G, an aphidicolin- and DAPI-induced common fragile site located at 2q31 region, was characterized by us using a FISH-based approach to identify a BAC contig of over 1 Mb that spans the fragile region (Limongi et al., 2003). Recurrent deletions, that may suggest the presence of TS genes, are observed at this region in some neoplasms, mostly leukemias and lymphomas (Mitelman et al., 2004). According to the human genome sequence public data base (http://www.ncbi.nih.gov/mapview/), to date twelve genes have been localized within the FRA2G region. In this work, nine of these genes have been investigated for biallelic deletions and loss of expression (LOE) in a panel of nineteen cancer cell lines, eight of which derived from leukemias and lymphomas

    Biallelic deletion and loss of expression analysis of genes at FRA2G common fragile site in tumor-derived cell lines.

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    Common fragile sites (CFS) are regions of chromosome instability that show gaps or breaks when cells are exposed to particular culture condition. Much evidence suggests that CFSs are causally related to cancer as breakpoints in recurrent chromosome mutations and as sites of viral integration. We investigated the FRA2G CFS (2q31) for biallelic deletions and loss of expression in a panel of 19 tumor-derived cell lines. We found that Burkitt lymphoma–derived cell line DAUDI has a biallelic deletion of eight of the nine analyzed genes. Moreover, we observed loss of expression (LOE) of the DHRS9 gene (alias RDHL), one of the deleted genes in the DAUDI cell line, in MOLT- 14 and Raji cell lines derived from Burkitt lymphoma and from T-cell acute lymphoblastic leukemia, respectively. DHRS9 is involved in development and differentiation pathways. I.F.: 1,6

    Fragile site FRA1H and transcriptional profiling of genes located within this region in tumor-derived cell-lines.

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    Common fragile sites (CFSs) are chromosome regions extending for hundreds or thousands of kilobases that exhibit gaps and breaks when the cells are exposed to replication stress and to some DNA binding compounds [1]. CFS (n=88) are located at specific loci on the chromosomes of all analysed individuals but the frequency of their expression varies among different individuals. Partial or complete molecular characterization of about twenty CFSs were performed but the basis of their fragility has not been definitively clarified. CFSs are regions of genomic instability frequently involved in sister chromatid exchanges in viral integrations and in chromosome mutations, and gene amplifications recurrent in cancer [rev. in 2]. In cancer cells, the analysis of the integrity and of the correct expression level of genes codified in the sequences of some characterized CFSs revealed in most of them the presence of rearrangements, loss of heterozygosity and modification or loss of expression of known or potential oncogenes and tumor suppressor genes [e.g. 3]. Recently, we analysed the FRA1H site (1q41-q42.1) [4] (Fig. 1). We found that it is one of the largest characterized CFSs extending over about 10 Mb. FRA1H is the first characterized CFS which expression is not induced by aphidicolin but instead by DAPI (4’,6-diamidino-2-phenylindole), by 5-azacytidine (5-azaC) and 5-azadeoxycytidine (5-azadC) and by infection of primary cells with adenovirus 12 (Ad12). Forty-nine genes are mapped at the FRA1H region. They include two microRNA (miRNA) genes, MIRN194-1 and MIRN215, codified as a cluster of 389 bp within an intron sequence of the gene IARS2, and two very large genes, USH2 (Usher syndrome 2A; 801 kb) and ESRRG (estrogen-related receptor gamma; 587 kb) (Fig. 2). Both miRNAs and very large genes have frequently been found located at fragile sites and there is evidence that the expression level or the structure of some of them are altered in cancer cells [5-8]. The FRA1H region is recurrently deleted in various neoplasms, mainly leukemias and lymphomas [9]. In this work, nine genes, localized in the FRA1H region, spaced to cover the complete CFS and with a possible role in transformation or regulation of cell proliferation, were investigated by PCR for homozygous deletions and by Real-time PCR for modifications or loss of gene expression in a panel of 19 cancer cell lines
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